Mismatch negativity impairment associated with alcohol consumption in chronic alcoholics: a scalp current density study.

Previous studies, based on amplitude and latency measurements of auditory event-related brain potentials, yielded inconclusive results about the status of mismatch negativity (MMN) in chronic alcoholics. The present study explores scalp current density (SCD) dynamics during MMN latency range in alcoholics, and correlates electrical SCD results with clinical data of the patients. SCD was computed from 30 electrodes in 16 abstinent chronic alcoholics and 16 healthy control volunteers in a paradigm on MMN elicited by duration changes. Reduced activity was observed in left frontal and right anterior and posterior temporal areas during MMN in alcoholics. Alcohol consumption correlated negatively with SCD intensity in these regions. Delayed activation was observed in the left posterior temporal area in the patients. Alcohol abstinence duration correlated positively with SCD intensity in this region. These results point to an impairment of automatic brain processing mechanisms associated with auditory change detection in chronic alcoholism. The present results suggest a reorganization of the computational neurodynamics of automatic auditory change detection linked to the amount of alcohol consumed in abstinent chronic alcoholics.

Auditory sensory memory as indicated by mismatch negativity in chronic alcoholism.

OBJECTIVES: A pre-conscious auditory sensory (echoic) memory of about 10 s duration can be studied with the event-related brain potential mismatch negativity (MMN). Previous work indicates that this memory is preserved in abstinent chronic alcoholics for a duration of up to 2 s. The authors' aim was to determine the integrity of auditory sensory memory as indexed by MMN in chronic alcoholism, when this memory has to be functionally active for a longer period of time. METHODS: The presence of MMN for stimuli that differ in duration was tested at memory probe intervals (MPIs) of 0.4 and 5.0 s in 17 abstinent chronic alcoholic patients and in 17 healthy age-matched control subjects. RESULTS: MMN was similar in alcoholics and controls when the MPI was 0.4 s, whereas MMN could not be observed in the patients when the MPI was increased to 5.0 s. CONCLUSIONS: These results provide evidence of an impairment of auditory sensory memory in abstinent chronic alcoholics, whereas the automatic stimulus-change detector mechanism, involved in MMN generation, is preserved.

Acute and chronic effects of alcohol on preattentive auditory processing as reflected by mismatch negativity.

Chronic alcoholism, a major worldwide health problem, is associated with a variety of neurocognitive changes in the afflicted individuals. The precise neurophysiological basis of these changes is not yet understood. Mismatch negativity (MMN) is a preattentive event-related potential component indexing cortical auditory memory traces and automatic change detection in the brain that can be used to study the neural basis of cognitive impairments in various neurodegenerative diseases. MMN studies have revealed that even a low dose of acute alcohol significantly impairs automatic change detection and involuntary attention shifting. Recent MMN results on chronic alcoholism in turn suggest that auditory sensory traces decay slightly faster and are substantially more vulnerable to the distracting effect of backward masking in alcoholics than in healthy subjects. Furthermore, chronic alcohol abuse might accelerate the age-related impairment of automatic change detection. There is also evidence that the MMN changes might predict impaired performance in behavioral memory and attention tasks in alcoholics. In MMN studies of detoxified alcoholics, however, many confounding factors have to be taken into account. For instance, postwithdrawal brain hyperexcitability might be associated with a slightly enhanced or accelerated MMN/MMNm (the magnetic equivalent of MMN). In sum, MMN and MMNm provide an objective noninvasive tool for exploring the neurophysiological functional deficits related to both acute alcohol intoxication and chronic alcoholism.

The individual replicability of mismatch negativity at short and long inter-stimulus intervals.

OBJECTIVES: The individual replicability of the mismatch negativity (MMN) event-related brain potential (ERP) was studied at two different inter-stimulus intervals (ISIs), to establish its potential value for routine clinical evaluation of sound discrimination and auditory sensory memory. METHODS: Ten healthy young subjects were presented sequences of 3 stimulus trains, in two recording sessions approximately 1 month apart. The stimuli in the trains were delivered at an ISI of 300 ms, whereas the inter-train intervals (ITIs) were 0.4 s and 4.0 s in different blocks. ERPs were averaged to standard (75 ms) and deviant (25 ms) tones started equiprobably the stimulus trains. RESULTS: Significant Pearson product-moment correlations coefficients were found between sessions at all scalp locations for the short ITI, when the MMN was quantified as the mean amplitude in the 100-200 ms latency window around its peak. However, none of the correlations reached significance for the longer ITI. CONCLUSIONS: MMN appears to be a reliable measure for single-case assessment and follow-ups when obtained at short ISIs and quantified as an integrated window of neuroelectric activation over a temporal span.

Mismatch negativity and auditory sensory memory in chronic alcoholics.

BACKGROUND & METHODS: Preattentive auditory processing and sensory memory were investigated by means of mismatch negativity (MMN) in a sample of 22 middle-aged abstinent chronic alcoholics and 25 age-matched healthy controls. Stimuli were presented at two inter-stimulus intervals (ISIs, 0.75 sec and 2.0 sec) in separate blocks. RESULTS: No significant differences in amplitude or latency of MMN were found between alcoholic and control subjects in either of the two ISI conditions. However, when age was included as a factor in the analysis, MMN amplitude was attenuated in chronic alcoholics who were older than 40 years of age. CONCLUSIONS: These results indicate that the automatic stimulus-change detector mechanism associated with MMN generation is impaired in chronic alcoholics over the age of 40, suggesting that the neurotoxic effects of chronic consumption of alcohol are more prone to appear after a critical age.

Mismatch negativity and auditory sensory memory evaluation: a new faster paradigm.

A new faster paradigm to measure the duration of auditory sensory memory, as indexed by mismatch negativity (MMN) suppression to stimuli presented at increasing inter-stimulus intervals (ISI), is proposed. Trains of three stimuli were delivered at very short ISI (300 ms). The inter-train interval varied according to the memory probe interval (MPI) tested. Trains started randomly with a deviant or standard stimulus (50% each), with their event-related brain potentials subtracted to obtain the MMN. The new paradigm provided MMNs identical to the conventional one at MPIs of 0.4 and 4.0 s in young subjects, and revealed MMN suppression when the MPI was increased to 5.0 s in older subjects. The new paradigm estimates auditory sensory memory duration in one-third the time of conventional MMN.

Metastatic arthropathy report of two cases and review of the literature.

Metastatic arthropathy has been rarely reported as a manifestation of solid tumors. It is characterized by a monoarticular involvement and is frequently the first feature of the malignant process; therefore, it may pose a diagnostic challenge. We report two new cases of metastatic carcinomatous arthritis: a patient with right-knee monoarthritis as a presenting feature of pancreatic carcinoma and another one with right-elbow monoarthritis, preceded by constitutional and pulmonary symptoms, secondary to metastasis of undifferentiated carcinoma. We also review the literature for well documented cases of metastatic arthropathy secondary to solid tumors. Metastatic arthropathy indicates a poor prognosis because of a wide spread of the tumor when it is diagnosed. We emphasize the need for increasing awareness of cancer as a cause of monoarthritis.